Journal of applied physiology
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Clinical Trial
Skeletal muscle capillary density and microvascular function are compromised with aging and type 2 diabetes.
Adequate muscle perfusion is required for the maintenance of skeletal muscle mass. Impairments in microvascular structure and/or function with aging and type 2 diabetes have been associated with the progressive loss of skeletal muscle mass. Our objective was to compare muscle fiber type specific capillary density and endothelial function between healthy young men, healthy older men, and age-matched type 2 diabetes patients. ⋯ In line, skeletal muscle capillary contacts were much lower in the older and older type 2 diabetic patients when compared with the young. Sidestream darkfield imaging showed a significantly greater thickness of the erythrocyte perfused boundary region in the type 2 diabetic patients compared with the young. Skeletal muscle capillary density is reduced with aging and type 2 diabetes and accompanied by impairments in endothelial glycocalyx function, which is indicative of compromised vascular function.
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Tibetans have been reported to present with a unique phenotypic adaptation to high altitude characterized by higher resting ventilation and arterial oxygen saturation, no excessive polycythemia, and lower pulmonary arterial pressures (Ppa) compared with other high-altitude populations. How this affects exercise capacity is not exactly known. ⋯ Maximum oxygen uptake was correlated directly to DL(CO) and inversely to the slope of mPpa-cardiac index relationships in both Sherpas and acclimatized lowlanders. We conclude that Sherpas compared with acclimatized lowlanders have an unremarkable aerobic exercise capacity, but with less pronounced pulmonary hypertension, lower ventilatory responses, and higher lung diffusing capacity.
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We examined the control of breathing, cardiorespiratory effects, and the incidence of acute mountain sickness (AMS) in humans exposed to hypobaric hypoxia (HH) and normobaric hypoxia (NH), and under two control conditions [hypobaric normoxia (HN) and normobaric normoxia (NN)]. Exposures were 6 h in duration, and separated by 2 wk between hypoxic exposures and 1 wk between normoxic exposures. Before and after exposures, subjects (n = 11) underwent hyperoxic and hypoxic Duffin CO2 rebreathing tests and a hypoxic ventilatory response test (HVR). ⋯ The LLS was greater in AMS-susceptible than in AMS-resistant subjects; however, LLS was alike between HH and NH. In AMS-susceptible subjects, fB correlated positively and Vt negatively with the LLS. We conclude that 6 h of hypoxic exposure is sufficient to lower the peripheral and central CO2 threshold but does not induce differences in cardiorespiratory variables or AMS incidence between HH and NH.
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Bronchopulmonary C fibers are the primary chemosensitive afferents in the lung. The activation of bronchopulmonary C fibers evokes the pulmonary chemoreflex, which is characterized by apnea, hypotension, and bradycardia and is a critical reflex that modulates cardiorespiratory responses under physiological and pathological conditions. The present study was designed to investigate whether the pulmonary chemoreflex is altered following acute cervical spinal injury. ⋯ To clarify whether the attenuation of the pulmonary chemoreflex in C2Hx animals is restricted to capsaicin-induced stimuli, or generally applied to other stimuli that excite bronchopulmonary C fibers, another bronchopulmonary C-fiber stimulant (phenylbiguanide) was used to evoke the pulmonary chemoreflex in spontaneously breathing rats. We observed that phenylbiguanide-induced apnea was also blunted in C2Hx animals, suggesting that the respiratory response induced by bronchopulmonary C-fiber activation was attenuated following acute cervical spinal Hx. The blunted inhibitory respiratory response may represent a compensatory respiratory plasticity to preserve the breathing capacity and may also reduce the capability of preventing inhaled irritants in this injured condition.
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Ventilatory insufficiency remains the leading cause of death and late stage morbidity in Duchenne muscular dystrophy (DMD). To address critical gaps in our knowledge of the pathobiology of respiratory functional decline, we used an integrative approach to study respiratory mechanics in a translational model of DMD. ⋯ In the diaphragm, this physiological shift is associated with the loss of sarcomeres in series (∼ 60%) and an increase in muscle stiffness (∼ 900%) compared with those of the nondystrophic diaphragm, as studied during perfusion ex vivo. In addition to providing much needed endpoint measures for assessing the efficacy of therapeutics, we expect these findings to be a starting point for a more precise understanding of respiratory failure in DMD.